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“High abundance proteins in serum and plasma (e.g., albumin) are routinely see more removed during proteomic sample processing as they can mask lower abundance proteins and peptides of biological/clinical interest. A common method of albumin depletion is based on immunoaffinity capture, and many immunoaffinity devices are designed for multiple uses. In this case, it is critical that the albumin captured on the affinity matrix is stripped from the column prior to regeneration of the matrix and processing of subsequent samples, to ensure no carryover and that maximal binding sites are available for subsequent samples. The current study examines the ability of a manufacturer’s

protocol to remove the proteins and peptides captured by an immunoaffinity spin column. The data presented in the current work illustrate the difficulty in completely removing albumin from the immunoaffinity device, and consequently, may explain the variability and decreased efficiency shown for this device in previous studies. In summary, the current data present important considerations for the implementation of multiple-use immunoaffinity devices for processing subsequent

clinical samples in a proteomic workflow.”
“Prostate cancer is the most prevalent cancer in men of the United States and Europe, and although current treatments have efficacy in treating primary prostate cancer, they are associated with a decreased quality of life and are find more ineffective in treating the metastatic disease. The identification of oncogenes associated with the formation, proliferation, and metastasis of prostate cancer has presented promising targets for RNA interference (RNAi)-based check details gene therapy. However, the potential of RNAi as a successful therapeutic depends on effective delivery. In this review, we discuss the potential of targeting oncogenes implicated in prostate cancer with RNAi-based therapeutics using non-viral bioresponsive ‘smart’ delivery systems that work in harmony with the physiological and biochemical environments of prostate tumours.”
“The effect of adiponectin and leptin on the proliferation of the human microvascular endothelial cell line

(HMEC-1) was studied in the absence or presence of fetal bovine serum (FBS). The participation of extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase/Akt (PI-3K/Akt) pathways in this effect were evaluated. We studied the effect of both adipokines on the motility, mitosis, proliferation and cell death processes of HMEC-1 cells using live-cell imaging techniques. Adiponectin but not leptin further increased the proliferative effect induced by FBS on HMEC-1. This effect seems to be the consequence of an increase in the mitotic index in adiponectin-treated cells when compared to untreated ones. The presence of either the mitogen-activated protein kinase (MAPK) inhibitor (PD98059), or PI-3K inhibitor (LY294002), reduced the effect of adiponectin in a dose-dependent manner.